Diseases in the body that are caused by vitamin B12 deficiency have several medical names:
- B12 deficiency anemia,
- Birmer-Addison disease
- Pernicious anemia.
- History of the disease
- ICB code 10
- Megaloblastic type of anemia
- What is common and what is the difference between the 2 types of megaloblastic anemias?
- Symptoms of anemia
- Forms of development
- B12 deficiency anemia in children
- Therapy for B12 deficiency anemia
- Complicated form of B12 deficiency anemia
- Diet for this form of anemia
- Life prognosis for B12 deficiency anemia
History of the disease
The history of the disease of this species goes back to 1855, when the British doctor Addison gave a detailed explanation of this disease, and in 1872 the German doctor Birmer supplemented the description of this pathology, and after that the lack of vitamin B12 began to be characterized as anemia, which is of a malignant nature.
At that time, there were no methods for the correct diagnosis of pathology, as well as qualified treatment, so hemoglobin went down to 30,0 and below g/l, the person fell into a coma, which led to death.
Only in the 20th century in 1926, a discovery was made, which was assessed by the Nobel Prize, that anemia with vitamin B12 deficiency is the inability of the stomach organ to produce a specific enzyme that helps the absorption of this vitamin from the digestive system.
Blood for B12-deficiency anemia
ICB code 10
According to the international classification of diseases of the tenth revision of ICD-10, this pathology belongs to class D 51, “Vitamin-B12-deficient anemia”.
Megaloblastic type of anemia
Pernicious (with B12 deficiency) anemia refers to the megaloblastic form of anemia, and is rarely combined with another megaloblastic folic deficiency anemia.
Megaloblastic anemia is a rather rare form of pathology in which there is a deviation from the normal absorption of the digestive system of folic acid, vitamin B12 and cyanocobalamin substances.
As a result, there is a lack of B vitamins in the body: B12 and B9.
Megaloblasts are modified red blood cells that are synthesized in cells by DNA and RNA. Megaloblasts appear in bone marrow cells as a consequence of an abnormality in the synthesis procedure. This is manifested in morphological changes in the composition of cells.
What is common and what is the difference between the 2 types of megaloblastic anemias?
Vitamins of group B enter the human body with products of animal origin. In the stomach, they bind to gastromucoprotein and are absorbed in the small intestine. For the normal functioning of the body, the daily dosage of vitamin B12 should be 7 μg.
The reserve of this vitamin is in the liver no more than 5 mg. The body’s need for folic acid is about 100 mcg per day. Vitamin B9 reserve up to 10 mg.
Violations in the synthesis of DNA molecules leads to the inability of these cells in the bone marrow to divide rapidly.
These cells include:
- Membranes of the mucous system,
- Digestive tract systems,
- Bone marrow cells,
- Skin cells.
The cells of the hematopoietic system (hematopoietic) are cells that multiply faster than others. Therefore, the indicators (reduced level of erythrocytes and low hemoglobin coefficient) in the hematopoietic system characterize the first manifestations of megaloblastic anemia.
With the manifestation of anemia, the following signs of the hemolytic nature of anemia are often observed:
- Pathology of thrombocytopenia, a decrease in the index in the blood of platelets,
- Disease neutropenia decreased leukocyte count of neutrophilic type,
- Blood pathology agranulocytosis decreased leukocyte count,
- Disease monocytosis – a decrease in monocyte molecules,
- Decreased synthesis of reticulocytes.
Difference and relationship between folate deficiency B9 anemia and B12 vitamin deficiency:
- Vitamin B12 is involved in the synthesis of folic acid molecules. The acid is part of the thymidine molecule, which is a component of the DNA molecule. With the well-coordinated work of these components, and with their required amount for the biochemical reaction, the normal formation of blood cells and cells for the normal functioning of the digestive tract occurs,
- The functional duties of vitamin B12 are to assist in the synthesis and breakdown of fatty acids in the body. With a deficiency of cyanocobalamin molecules, a violation of the coordinated reaction occurs, and methylmalonic acid is deposited, which has a detrimental effect on the atoms of neurons. There is also a decrease in the synthesis of myelin, which forms a sheath for the fibers of nerve cells.
Folic acid is not involved in the breakdown of fatty acids and is not involved in the formation of sheaths for nerve fibers.
With a deficiency of vitamin B12, the doctor prescribes taking medications with folic acid, then it activates erythropoiesis, but only until this acid becomes in excess in the body.
With an overdose of folic acid, the following occurs:
- Disorder in the nervous system
- Degenerative changes in the bone spinal cord,
- Combined sclerosis with loss of motor functions,
- Funicular type of myelosis.
Symptoms of anemia
Symptoms of B12 deficiency anemia and folic acid (as well as its lack) are classified according to the following directions in the manifestation of pathology:
- Anemic syndrome in the hematopoietic system,
- Gastroenterological symptoms of disorders in the digestive tract,
- Neurological in nature,
- Symptoms in violation of the structure of the brain.
The classification of the anemic direction is manifested in the following symptoms:
- Great dizziness
- Weakness of the whole body
- Fainting state
- Rapid contraction of the heart muscle (sinus type tachycardia),
- Painful sensations in the chest,
- Noise in ears,
- Ambiguity in the perception of objects by the organs of vision,
- Yellow tint of the skin (the shade gives a high level of bilirubin in the blood).
- Unreasonable lack of need for food intake,
- Sudden weight loss
- Severe nausea that goes into vomit from the body
- The process of inflammation of the oral cavity,
- A burning sensation on the tongue
- The tongue takes on a crimson hue
- Birmer anemia Addison-Birmer disease
- Mild tingling in fingers and toes
- Constant chills
- Unsteadiness in motion
- Numbness in the lower limbs
- Lethargy legs
- The sensitivity of the skin disappears,
- Difficulty moving.
Abnormalities in the brain of this type of anemia, as well as disorders in the functioning of the spinal cord:
- Lack of memory
- A state of being lost
- Feeling of constant irritation
- Coma state,
- Cramps in the muscles.
With anemia, vitamin B12 deficiency, as well as with iron deficiency anemia, there are signs of severe hypoxia in the body:
- Pale skin tone
- Peeling on the skin,
- Angina pectoris,
- Sternum pain.
Forms of development
The pathogenesis of anemia with insufficient disappearance of B vitamins, namely B12 and B9, into the body, which affects the level of hemoglobin molecules, which is located in erythrocytes and is responsible for the delivery of oxygen atoms to all cells of the human body.
Anemia is divided into forms according to the index in the composition of blood plasma of hemoglobin molecules.
The lower the hemoglobin index, the more severe the course of the deficiency pathology:
- Light stage of development and course of hemoglobin index from 90,0 to 110,0 grams per liter of biological fluid,
- Moderate severity hemoglobin index from 70,0 to 90,0 grams per liter of blood plasma,
- The severe stage of the course of this pathology, the coefficient of red pigment does not exceed 70,0 and decreases even below this indicator.
The standard indicators of the amount of hemoglobin in the blood in men are 130,0 160,0 g/l.
B12 deficiency anemia in children
The main types of etiology of anemia with a lack of this vitamin in childhood are:
- Changes in the microflora of the baby,
- There is not enough of this vitamin in the child’s body,
- The presence of worms in the body,
- Castle factor during the period of intensive growth of the child.
Clinical indicators and manifestations of this type of pathology are similar to those of an adult, but there are characteristic symptoms in a child’s body:
- Severe dental caries from a young age
- Persistent stomatitis that begins in infancy
- Changes in the eyeball
- Changes in the nail plate, the plate is weak, brittle,
- Impaired attention and intelligence; decreased school performance.
In the decoding of the results of the clinical laboratory, the following values are:
- Low hemoglobin index,
- Reduced number of erythrocyte molecules,
- The chromaticity index is increased by more than 1,5,
- In the molecules of erythrocytes, the Kebot rings, as well as Jolly bodies, are present in such an amount that they are determined by analysis,
- Reticulocytes are increased
- Increased lymphocyte count,
- Platelets, as well as leukocytes in small quantities,
- Biochemistry revealed megaloblasts in the bone marrow puncture.
To help laboratory indicators, to establish the diagnosis of B12 deficiency anemia, an instrumental method for diagnosing the child’s body is used:
- Ultrasound of liver cells,
- Spleen cells ultrasound,
- Gastroendoscopy of the alimentary tract and intestines,
- Irrigoscopy of the small part in the intestine,
- Colonoscopy checks the condition of the colon.
Treatment of anemia in a child with B12 deficiency consists in saturating the body cells with these vitamins. Medicinal vitamin course 15 calendar days. A high-calorie diet is also prescribed, in which foods with vitamin B12 and folic acid are present.
To replenish the vitamin molecules in the body, the drug Cyanocobalamin is prescribed. The initial dosage of this drug is from 30,0 mcg to 50,0 mcg, when taken daily. This drug is injected inside.
The dosage is calculated individually by the treating doctor. The drug course is carried out in children under the strict supervision of a specialized specialist.
After the end of the course of treatment for prophylactic purposes and as a maintenance treatment, 100,0 250,0 mcg 2 times a month.
The standard indicators of the vitamin cyanocobalamin in the child’s body:
the age of the child, the norm per day of vitamin cyanocobalamin
|from birth to 6 months of age||0,40 μg|
|from 6 calendar months to one year||0,50 μg|
|at the age of one and up to 3 years||1,0 μg|
|from 3 calendar years to 6 years||1,50 μg|
|from the age of six to the age of 10||2,0 μg|
Vitamin B12 benefits the body when it is absorbed in the intestines. For the reaction of this absorption to occur, an enzyme is needed, which is produced by the internal parts of the stomach, the Castle’s enzyme.
Without the formation of an enzyme, the vitamin B12 molecule is excreted outside the body without getting it for biochemical processes, through feces.
In case of B12 deficiency anemia, Castle’s enzyme is not synthesized in the stomach, therefore, the vitamin that enters the food is also not absorbed through the intestines.
There is a supply of vitamin B12 molecules in the liver cells, which, if used wisely, can be sufficient for 5 calendar years. As a result, anemia occurs after a while, after the stomach has ceased to produce this factor.
Castle factor deficiency is the main cause of the pathology of B12 deficiency anemia.
The lack of cyanocobalamin is caused by the following factors:
- Low content of foods with vitamin B12 in food (main reason). Cyanocobalamin is found in animal products. Vegetarianism is the main risk factor for B12 deficiency in food.
- The function of the Castle factor is impaired. With atrophy of the cells of the mucous membranes, the functionality of the intrinsic factor does not manifest itself, or it decreases. This cause of atrophy is genetic, congenital, with gastritis of the stomach, with exposure to the stomach of toxic elements (intoxication of the body), as well as the effect on the antibody factor,
- Absence, or partial loss of receptors that are necessary for the factor. This pathology develops with Crohn’s disease, with neoplasms in the small intestine (cancer), with tuberculosis disease, with intestinal infantilism, as well as with enteritis in the chronic stage of the pathology,
- Absorption of B12 molecules by worms and pathogenic microorganisms. It is necessary to treat this pathology with therapy against competitors that absorb cyanocobalamin,
- With pathology of the pancreas. With this pathology, there is a deviation in the breakdown of protein protein, which is a link between the factor and vitamin B12,
- Genetic hereditary congenital anomaly is a reduced rate of transcobalamin synthesis in the body, which leads to a disruption in the transport of cyanocobalamin molecules to bone marrow cells.
For folate deficiency anemia, food etiology is not suitable, because vitamin B9 is present in every food of plant and animal origin. This B vitamin does not need the help of a factor and is absorbed on its own.
Folio deficiency problems begin when the following reasons appear in the body:
- Poor diet
- Small food intake,
- Old age of the patient, at this age there is a difficult assimilation of vitamins from food,
- Reception of alcoholic beverages. With alcohol addiction, a person cannot eat well,
- Pathology in the intestine that prevents vitamins from being absorbed by the body,
- Crohn’s disease
- Blood hemogram,
- Celiac disease pathology,
- Malignant neoplasms in the intestine,
- Increased need for vitamin B12 and folic acid in a woman during the period of intrauterine formation of the baby. In pregnant women, the consumption of these products with food should be increased, in order to avoid fetal hypoxia,
- Increased consumption of B9 in psoriasis pathology,
- When taking anticonvulsant medications, vitamin B9 and B12 deficiency occurs.
Vitamin deficiency occurs when taking medications
When making this diagnosis of B12 deficiency anemia, the doctor first of all, when diagnosing, collects an anamnesis when and under what circumstances there was a pronounced symptomatology of anemia, with its weakness and manifestations of pathology in the process of digestion.
It is also necessary to find out whether the patient has diseases that occur in the chronic stage, as well as to provide information about possible genetic hereditary congenital diseases.
After the anamnesis, the patient’s skin is examined, and pronounced symptoms on the skin are determined.
The doctor also measures the blood pressure index (in case of anemia, the pressure is lowered), as well as the heart rate (often the pulse is rapid).
After this examination, based on external signs, laboratory diagnostics (blood test) are assigned, as well as a list of instrumental studies:
- General blood analysis,
- Biochemical analysis of blood composition,
- Urine for general analysis,
- Bone marrow puncture,
- Electrocardiography (ECG),
- Ultrasound of the liver and spleen,
- Bowel ultrasound,
- Ultrasound of the stomach.
When decoding the general analysis, the whole picture of blood is visible, the indicators of each element in its composition. According to this analysis, with anemia of vitamin B12 deficiency, a decrease in erythrocyte molecules, as well as a reduced synthesis of reticulocytes, is seen.
The level of red pigment (hemoglobin) is reduced, platelets are also reduced, which provokes hypoxia. The chromaticity increases with anemia and reaches more than 1,50 (with a norm of 0,860 1,050).
During the analysis, the presence of proteins in urine is observed, and the possible detection of concomitant pathologies.
Biochemistry is the most valuable test for detecting abnormalities in the structure and composition of blood.
As part of biochemistry, the following indicators are detected in B12 deficiency anemia:
- Cholesterol index often elevated with anemia,
- The presence of creatinine,
- Blood glucose
- Uric acid,
- Electrolyte indicators of calcium, potassium and sodium molecules,
- Lactate dehydrogenase is an enzyme in the liver cells that promotes the absorption of iron by cells. Indicator of biological reactions for the synthesis of erythrocytes and hemoglobin,
- B vitamins are reduced. The B12 index is low.
The blood hemogram shows the hematocrit number, the percentage of all types of leukocytes is set by the leukocyte formula.
Myelogram, or indicators of bone marrow puncture, determines the level of production of erythrocyte molecules, as well as megaloblasts in the blood, which confirms the megaloblastic nature of hematopoiesis in the human body.
The instrumental technique determines the deviations from the normative indicators for the structure of internal organs, and also reveals violations in their functionality.
Therapy for B12 deficiency anemia
Therapy of B12 deficiency anemia begins with the treatment of the root cause of this deficiency, this is therapeutic therapy for the destruction of worms, normal and balanced nutrition, as well as a surgical method for treating malignant neoplasms.
For the complex treatment of anemia, the drug B12 is administered into the body at a dosage of 200,0 μg 250,0 μg per day. The drug is injected into the muscle tissue, or injected under the skin of the human body.
If anemia has affected the centers of the nervous system, then the drug therapy regimen is as follows for the first 3 calendar days, the dosage of the vitamin is 1000,0 mcg per day, and the subsequent treatment is according to the prescribed scheme. The treatment regimen, as well as the dosage of B12, is prescribed by the attending doctor and depends on the degree of vitamin B12 deficiency in the body, which caused the anemia.
After stabilization of this vitamin in the body, to maintain it at a normal level, the drug B12 is used in the treatment at 100,0 μg 200,0 μg 1 time per calendar month.
Clinical recommendations for the rapid replenishment of erythrocytes in the blood, the introduction of intravenous erythrocyte mass, which can restore the destroyed balance in the blood plasma of the human body.
Complicated form of B12 deficiency anemia
If you do not take emergency measures in treatment, the consequences of this type of anemia can be quite serious and pose a threat to the patient’s life:
- Comatose state in which the patient does not respond to external stimuli. Coma can occur from cerebral hypoxia with anemia and can cause death,
- A severe degree of anemia, which significantly worsens the condition of the body and triggers irreversible consequences in it. This degree occurs when the hemoglobin index is lower than 70,0 g/l,
- Funicular myelosis is a lesion of the cells of the spinal cord, as well as the nerve endings of the peripheral parts of the body. Damage to the connective nerve fibers of the spinal cord with the centers of the brain, as well as with all internal organs and body systems. With these violations, the sensitivity of the limbs decreases, unsteadiness appears in movements, and the period of progression of myelosis, the sensitivity disappears altogether and the person is not capable of independent movement,
- Destruction of cells of internal organs, which subsequently leads to non-functionality of this organ (heart, liver and spleen cells, digestive tract, kidney cells, respiratory system are affected).
If the treatment process began too late, then complications in the nervous system cannot be restored. These destruction are irreversible.
Prevention is mainly aimed at improving B12 intake through foods:
- Eating animal products with a large amount of B12 in them,
- Timely therapy of pathologies that can cause B12 deficiency and provoke anemia,
- After surgery on the organs of the digestive tract, take medications to maintain the level of this vitamin.
Vitamin B12-rich foods
Diet for this form of anemia
A balanced diet is especially necessary during the period of intrauterine development of a child, since the formation of an infant depends on the intake of vitamins in a pregnant woman’s body, as well as the occurrence of intrauterine pathologies that are revealed after birth.
During pregnancy, the need for vitamin B12 increases by 50,0%.
products; amount of B12 in μg
|Calf liver||· 60,0|
|Liver of a young pig||· 30,0|
|Chicken liver||· 16,0|
|Mackerel fish||· 12,0|
|Rabbit meat||· 4,30|
|Fish perch||· 2,40|
|Fat sour cream|
In case of B12 deficiency anemia, diet table number 11 is used. This diet should increase the content of protein and vitamin B12 in the body. The method of cooking food is common. You need to eat 5 times a day.
Energy value of diet number 11:
- Proteins 110,0 grams 130,0 grams (60,0% animal origin, 40,0% vegetable),
- Fat 100,0 grams 120,0 grams (80,0% animal and only 20,0% vegetable),
- Carbohydrates 400,0 grams 450,0 grams,
- Salt not more than 15,0 grams,
- Purified water 1,5 liters.
products useful for anemia B12 deficiency; prohibited foods
|Veal, pork, chicken liver||Milk|
|· butter||Confectionery sweet products|
|Meat: veal, rabbit, pork||Drinks with caffeine|
|Eggs||· Coca Cola|
|Fat sour cream||Alcoholic drinks|
|Fat-free cottage cheese||Do not use vinegar in cooking|
|· hard cheese||Sugary carbonated drinks|
|Legumes: peas, lentils|
|Vegetables: carrots, potatoes, cabbage, beets, tomatoes|
|Fruits of all sorts|
|Berries of all types|
|Vegetables with a green color are rich in iron|
Life prognosis for B12 deficiency anemia
Favorable prognosis; Poor prognosis
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